Nosocomial Pneumonia (Hospital-Acquired & Ventilator-Associated)
Hospitalized patients carry different flora with different resistance patterns than healthy patients in the community, and their health status may place them at higher risk for more severe infection. The diagnostic approach and antibiotic treatment of patients with HAP is, therefore, different from patients with Community Acquired Pneumonia (CAP). Similarly, management of patients in whom VAP develops following endotracheal intubation and mechanical ventilation should address issues specific to this group of patients.
Considered together, these nosocomial pneumonias (HAP/VAP) represent an important cause of morbidity and mortality despite widespread use of preventive measures, advances in diagnostic testing, and potent new antimicrobial agents. HAP is the second most common cause of infection among hospital inpatients and is the leading cause of death due to infection with mortality rates ranging from 20% to 50%.
While a minority of cases occurs in ICU patients, the highest-risk patients are those in ICUs or who are being mechanically ventilated; these patients also experience higher morbidity and mortality from HAP. Definitive identification of the infectious cause of a lower respiratory infection is rarely available on presentation, thus, rather than pathogendirected antibiotic treatment, the choice of empiric therapy is usually informed by epidemiologic and patient data.
Definition & Pathogenesis
HAP develops more than 48 hours after admission to the hospital and VAP develops in a mechanically ventilated patient more than 48 hours after endotracheal intubation.
Three factors distinguish nosocomial pneumonia from CAP:
- different infectious causes;
- different antibiotic susceptibility patterns, specifically, a higher incidence of drug resistance; and
- poorer underlying health status of patients putting them at risk for more severe infections.
Since access to the lower respiratory tract occurs primarily through microaspiration, nosocomial pneumonia starts with a change in upper respiratory tract flora. Colonization of the pharynx and possibly the stomach with bacteria is the most important step in the pathogenesis of nosocomial pneumonia.
Pharyngeal colonization is promoted by exogenous factors (eg, instrumentation of the upper airway with nasogastric and endotracheal tubes; contamination by dirty hands, equipment, and contaminated aerosols; and treatment with broad-spectrum antibiotics that promote the emergence of drug-resistant organisms) and patient factors (eg, malnutrition, advanced age, altered consciousness, swallowing disorders, and underlying pulmonary and systemic diseases). Within 48 hours of admission, 75% of seriously ill hospitalized patients have their upper airway colonized with organisms from the hospital environment. Impaired cellular and mechanical defense mechanisms in the lungs of hospitalized patients raise the risk of infection after aspiration has occurred.
Gastric acid may play a role in protection against nosocomial pneumonias. Observational studies have suggested that elevation of gastric pH due to antacids, H2 -receptor antagonists, proton-pump inhibitors (PPIs), or enteral feeding is associated with gastric microbial overgrowth, tracheobronchial colonization, and HAP/VAP. Sucralfate, a cytoprotective agent that does not alter gastric pH, is associated with a trend toward a lower incidence of VAP. The Infectious Diseases Society of America and other professional organizations recommend that acid-suppressive medications (H2 -receptor antagonists and PPIs) be given only to patients at high risk for stress gastritis.
The microbiology of the nosocomial pneumonias differs from CAP but is substantially the same among HAP and VAP. The most common organisms responsible for HAP include S aureus (both methicillin-sensitive S aureus and MRSA), P aeruginosa, gram-negative rods, including nonextended spectrum beta-lactamase (non-ESBL)–producing and ESBL-producing (Enterobacter species, K pneumoniae, and Escherichia coli) organisms.
VAP patients may be infected with Acinetobacter species and S maltophilia. Anaerobic organisms (bacteroides, anaerobic streptococci, fusobacterium) may also cause pneumonia in the hospitalized patient; when isolated, they are commonly part of a polymicrobial flora. Mycobacteria, fungi, chlamydiae, viruses, rickettsiae, and protozoal organisms are uncommon causes of nosocomial pneumonias.
Symptoms and Signs
The symptoms and signs associated with nosocomial pneumonias are nonspecific; however, two or more clinical findings (fever, leukocytosis, purulent sputum) in the setting of a new or progressive pulmonary opacity on chest radiograph were approximately 70% sensitive and 75% specific for the diagnosis of VAP in one study. Other findings include those listed on CAP.
The differential diagnosis of new lower respiratory tract symptoms and signs in hospitalized patients includes heart failure, atelectasis, aspiration, ARDS, pulmonary thromboembolism, pulmonary hemorrhage, and medication reactions.
Diagnostic evaluation for suspected nosocomial pneumonia includes blood cultures from two different sites. Blood cultures can identify the pathogen in up to 20% of all patients with nosocomial pneumonias; positivity is associated with increased risk of complications and other sites of infection. Blood counts and clinical chemistry tests do not establish a specific diagnosis; however, they help define the severity of illness and identify complications. The assessment of oxygenation by an arterial blood gas or pulse oximetry determination helps define the severity of illness and determines the need for assisted ventilation. Thoracentesis for pleural fluid analysis should be considered in patients with pleural effusions.
Examination of lower respiratory tract secretions is attended by the same disadvantages as in CAP. Gram stains and cultures of sputum are neither sensitive nor specific in the diagnosis of nosocomial pneumonias. The identification of a bacterial organism by culture of lower respiratory tract secretions does not prove that the organism is a lower respiratory tract pathogen. However, it can be used to help identify bacterial antibiotic sensitivity patterns and as a guide to adjusting empiric therapy
When HAP is suspected in a patient who subsequently requires mechanical ventilation, secretions obtained by spontaneous expectoration, sputum induction, nasotracheal suctioning, and endotracheal aspiration should be cultured. For patients with suspected VAP, endotracheal aspiration using a sterile suction catheter with semi-quantitative cultures of lower respiratory tract secretions is the recommended method of evaluation.
The initial treatment of HAP and VAP is usually empiric, based on risk factors for MRSA and multiple drug-resistant pathogens as well as local antibiograms and mortality risk. Each hospital should generate antibiograms to guide the optimal choice of antibiotics with the goals of reducing exposure to unnecessary antibiotics and the development of antibiotic resistance and thus minimizing patient harm.
Because of the high mortality rate, therapy should be started as soon as pneumonia is suspected. After results of sputum, blood, and pleural fluid cultures are available, it may be possible to change initially broad to more specific therapy.
Endotracheal aspiration cultures have significant negative predictive value but limited positive predictive value in the diagnosis of specific infectious causes of HAP/VAP. If an invasive diagnostic approach to suspected VAP using quantitative culture of bronchoalveolar lavage (BAL), protected specimen brush (PSB), or blind bronchial sampling (BBS) is used, antibiotics can be withheld when results are below a diagnostic threshold (BAL less than 104 CFU/mL, PSB or BBS less than 103 CFU/mL).
Duration of antibiotic therapy should be individualized based on the pathogen, severity of illness, response to therapy, and comorbid conditions. Data from one large trial assessing treatment outcomes in VAP suggested that 8 days of antibiotics is as effective as 15 days, except in cases caused by P aeruginosa.